Analysis of the role of the QseBC two-component sensory system in epinephrine-induced motility and intracellular replication of Burkholderia pseudomallei
2
Issued Date
2023-02-01
Resource Type
eISSN
19326203
Scopus ID
2-s2.0-85148682963
Pubmed ID
36821630
Journal Title
PLoS ONE
Volume
18
Issue
2 February
Rights Holder(s)
SCOPUS
Bibliographic Citation
PLoS ONE Vol.18 No.2 February (2023)
Suggested Citation
Meethai C., Vanaporn M., Intarak N., Lerdsittikul V., Withatanung P., Janesomboon S., Vattanaviboon P., Chareonsudjai S., Wilkinson T., Stevens M.P., Stevens J.M., Korbsrisate S. Analysis of the role of the QseBC two-component sensory system in epinephrine-induced motility and intracellular replication of Burkholderia pseudomallei. PLoS ONE Vol.18 No.2 February (2023). doi:10.1371/journal.pone.0282098 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/82738
Title
Analysis of the role of the QseBC two-component sensory system in epinephrine-induced motility and intracellular replication of Burkholderia pseudomallei
Other Contributor(s)
Abstract
Burkholderia pseudomallei is a facultative intracellular bacterial pathogen that causes melioidosis, a severe invasive disease of humans. We previously reported that the stress-related catecholamine hormone epinephrine enhances motility of B. pseudomallei, transcription of flagellar genes and the production of flagellin. It has been reported that the QseBC two-component sensory system regulates motility and virulence-associated genes in other Gram-negative bacteria in response to stress-related catecholamines, albeit disparities between studies exist. We constructed and whole-genome sequenced a mutant of B. pseudomallei with a deletion spanning the predicted qseBC homologues (bpsl0806 and bpsl0807). The ΔqseBC mutant exhibited significantly reduced swimming and swarming motility and reduced transcription of fliC. It also exhibited a defect in biofilm formation and net intracellular survival in J774A.1 murine macrophage-like cells. While epinephrine enhanced bacterial motility and fliC transcription, no further reduction in these phenotypes was observed with the ΔqseBC mutant in the presence of epinephrine. Plasmid-mediated expression of qseBC suppressed bacterial growth, complicating attempts to trans-complement mutant phenotypes. Our data support a role for QseBC in motility, biofilm formation and net intracellular survival of B. pseudomallei, but indicate that it is not essential for epinephrine-induced motility per se.